Dual antiplatelet therapy in a patient with simultaneous aneurysmal subarachnoid hemorrhage and myocardial infarction.

BACKGROUND: Electrocardiography (ECG) changes after subarachnoid hemorrhage (SAH) are well described. However, concurrent myocardial infarction (MI) and SAH are rarely reported, and its management remains a dilemma. We report a patient with traumatic SAH concurrent with acute MI that managed successfully by endovascular intervention and dual antiplatelet therapy. CASE DESCRIPTION: A 47-year-old man was admitted to the emergency department with a complaint of severe headache. Diffuse SAH, with a Hunt and Hess score of 5, was noticed. ECG showed ST elevation in anterior leads, and cardiac troponin became positive. On brain computed tomography angiogram, a 6 mm anterior communicating artery aneurysm was seen. Considering the possibility of MI and SAH simultaneously, endovascular obliteration of the aneurysm was done, and then, the patient received dual antiplatelet medications until coronary angiography was done. Coronary angiography revealed normal epicardial coronary arteries. The patient was discharged with a Glasgow Coma Scale score of 15 and was visited 2 months after discharge without any new episodes of intracranial hemorrhage with a modified Rankin scale score of 2.
CONCLUSION: Cerebral aneurysm coiling could be considered as the first choice of treatment in the case of acute MI with hemodynamic stability, before carrying out cardiac endovascular intervention or antiplatelet medication to reduce the risk of rebleeding from a brain aneurysm. Copyright:

INTRODUCTION

Electrocardiography (ECG) and echocardiographic changes such as nonspecifc ST deviations, T-wave inversion, prolonged QT interval, and transient segmental hypokinesis of the left ventricular wall frequently report in accompany with subarachnoid hemorrhage (SAH). However, the association between SAH and acute myocardial infarction (MI) is rarely reported.[1]

We report a patient with traumatic SAH concurrent with acute MI that managed successfully by endovascular intervention and dual antiplatelet therapy.

CASE REPORT

A 47-year-old cocaine-addicted man with a history of severe headache following falling was referred to the emergency department with a complaint of decreased level of consciousness and intubated with a Glasgow Coma Scale (GCS) score of 4. No lateralizing signs were observed, and the pupils were symmetrical and midsize. Brain computed tomography (CT) scan showed diffuse SAH with a Hunt and Hess score of 5 and the World Federation of Neurosurgical Societies (WFNS)[1] score of 5. On further workup, the patient’s ECG showed ST elevation in V1-4 and ST depression in inferior leads. Cardiac troponin also raised significantly along with the evidence of wall motion abnormality on echocardiography. According to the patient’s neurologic condition, the treatment of possible MI was started with the dual oral antiplatelet drug.

Brain CT angiogram that performed after admission of the patient to the neurosurgical intensive unit, revealed a 6 mm AComA aneurysm. Single antiplatelet therapy was started on the 1st day after the ictus with no new episode of rebleeding from the AComA aneurysm. Given the evidence of SAH and aneurysm on CT, the administration of dual antiplatelet drugs and anticoagulants imposed a high risk of rebleeding and deteriorating neurologic condition on our patient. Therefore, considering the stability of our patient’s hemodynamic, we decided to close the aneurysm first. Cerebral angiography was performed to obtain anatomical data required for endovascular treatment [Figure 1a and b]. The endovascular intervention was done, and complete occlusion was achieved [Figure 1c].

Figure 1:

Angiography of anterior communicating artery aneurysm (a), roadmap image of AComA aneurysm on angiography (b) and postcoiling image of aneurysm (c).

After successful endovascular closure of brain aneurysm, dual antiplatelet therapy was started with no evidence of rebleeding on follow-up brain CT. The patient underwent coronary angiography that revealed normal epicardial coronary arteries that result in discontinuing antiplatelet therapy. Five days later, the patient was discharged with a GCS score of 15 and was visited 2 months after discharge without any new episodes of intracranial hemorrhage and modified Rankin scale score of 2.

DISCUSSION

SAH can be associated with ECG changes.[6] The most common ECG changes in SAH include nonspecific ST deviation, T-wave inversion, and prolonged QT interval caused by cardiocerebral interaction.[2] ECG changes followed by SAH can be mistaken for MI. However, cardiac changes in SAH are not limited to ECG changes and cardiac motility, and even enzymes could occur. Cardiac dysfunction following aneurysmal SAH includes dysrhythmias, infarction, ischemia, and stunned myocardium with ventricular dysfunction.[4,10]

It is reported that elevated cardiac markers may be seen in patients with SAH.[8] The etiologies for these changes are not well known. Takotsubo cardiomyopathy, acute pericarditis, and MI are the proposed mechanisms for these changes.[3] Diagnosis of the etiology of ECG changes is of great importance because the mainstay of treatment in MI is fibrinolytic and/or antiplatelet medications, which are both contraindicated in acute SAH. In our case, the patient was presented with loss of consciousness and admitted due to SAH. However, evidence of ST elevation was observed on ECG after admission. We propose two possibilities for ECG changes in our patient; the first was ECG changes secondary to the cerebral hemorrhagic event, and the second was coronary artery spasm secondary to cocaine abuse in our patient.

A review of the literature showed only three cases of concomitant MI and SAH in patients with a decreased level of consciousness.[7,9] In Tan et al. report, the patient admitted with cardiac manifestation and then developed SAH. However, they believe that SAH was the initial event that causes secondary coronary plaque rupture. Unlike our management strategy, they chose dual antiplatelet therapy in the first step due to the high risk of coronary stent thrombosis.[7] van der Velden et al. discussed a treatment protocol for patients with concomitant MI and SAH. Platelets and their coagulation factors play a significant role in the development of clinical vasospasm.[9] They showed that antiplatelet therapy could be started as soon as 72 h after SAH or after coiling of the aneurysm.[9]

Nagahama et al. showed that treatment with an antiplatelet agent led to a decrease of vasospasm and poor outcome. Their results strongly suggest that antiplatelet reduces the risk of clinical vasospasm in patients with SAH without an increased risk of hemorrhagic complications.[5]

According to our experience, cerebral aneurysm coiling could be considered as the first choice of treatment in the case of confronting the possibility of MI and hemodynamic stability, before carrying out cardiac endovascular intervention or antiplatelet medication to reduce the risk of rebleeding from a brain aneurysm, and it should be performed in the first 72 h after the ictus. We followed this treatment strategy successfully, and our patient did not have any evidence of vasospasm. However, further studies with more patients are needed to identify actual outcomes and potential risks.

CONCLUSION

Discontinuation of life-saving anti-thrombotic agents or life-threatening worsening of neurological conditions without discontinuing these medications is a challenge in the management of myocardial infarction coincidence with subarachnoid hemorrhage. Our experience provides a suggestion that proceeding with anti-thrombotic agents after invasive management of brain pathology might show promising results.